Salicylates commonly cause tinnitus, deafness, nausea and vomiting (salicylism). Hyperventilation results from stimulation of respiratory centre.

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1 Aspirin poisoning CLINICAL FEATURES Salicylates commonly cause tinnitus, deafness, nausea and vomiting (salicylism). Hyperventilation results from stimulation of respiratory centre. Severe poisoning causes metabolic acidosis, delirium and coma, though impaired consciousness uncommon in adults. SERUM LEVELS Serum salicylate should be measured in all those with symptoms. Arterial gases indicated in clinically severe poisoning and in adults with levels > 3.26mmol/l (initially respiratory alkalosis, later metabolic acidosis). GENERAL MANAGEMENT Empty stomach by gastric lavage if more than 4.5 g taken by an adult within 1hour. Give 50 g activated charcoal. MINOR TOXICITY 1. Adults with levels <3.26 mmol/l do not usually require more than an increase in oral fluid intake and a single dose (50 g) of activated charcoal. MODERATE TOXICITY Unlikely to occur if <300 mg/kg Aspirin taken (ie 70x300 mg tablets in a patient weighing 70 kg). Adults with level between 3.26 and 5.07 mmol/l should have 50 g charcoal every 4 hours with lactulose until clinical improvement/drop in serum salicylate, together with measures to alkalinise the urine. Alkalinisation best achieved by 1.5 litres of 1.26% sodium bicarbonate over 3 hours. Check by testing urine with litmus paper. Beware hypokalaemia when alkaline diuresis is successful. Forced diuresis is not indicated. SEVERE POISONING If levels exceed 5.07 mmol/l or there is severe acidosis or features of neurotoxicity (delirium, extreme agitation, confusion, coma and convulsions) then mortality is about 5% and patients should be discussed with poisons unit and considered for haemodialysis. Acidosis should be corrected as a matter of urgency. Forced diuresis may precipitate fatal pulmonary oedema and is contraindicated.

2 Other poisoning TRICYCLIC ANTIDEPRESSANTS If HR <100 & pupils not dilated then unlikely to be significant OD. QRS >120 msec predicts dysrhythmia, fits and coma - telemetry not needed if QRS < 120 msec. Advise gastric washout if presents within 1 hour. Give multidose charcoal if QRS > 120 msec. If patient develops dysrhythmia - correct electrolytes and hypoxia and avoid anti-arrhythmics if possible. 50 ml 8.4% sodium bicarbonate IV may correct dysrhythmia even if not acidotic and can be repeated (probably works by hypertonicity of saline). VT with compromise - try DC shock after adequate sodium bicarbonate given. SVT with compromise - try short acting betablocker eg esmolol. OPIATE POISONING Give Naloxone mg IV to wake patient up. If second dose Naloxone required then start infusion. For infusion 2/3 the dose required to wake patient up is given per hour to keep patient sufficiently awake but not agitated & wanting to leave. DIGOXIN POISONING Digoxin may be inactivated by specific antibody fragments (Digibind). Digibind not usually given on basis of serum level alone with should be reserved for patients with toxic serum level and either hypotension, heart block or VT. NON-STEROIDAL ANTI INFLAMATORY DRUGS Give activated charcoal if >10 tablets ingested by an adult. Main risk is of seizures - Give IV Diazepam (10 mg for an adult). NSAIDs have short half life usually safe to discharge within 12 hours. SELECTIVE SEROTONIN RE-UPTAKE INHIBITORS (SSRIS) Include Fluoxetine, Paroxetine, Citalopram, Sertraline and Fluvoxamine. Tend to be less toxic than tricyclic antidepressants in overdose. Give single dose of charcoal if > 10 tablets have been taken. Cardiac monitoring needed if > 10 tablets taken & HR >100/min. No known benefit from sodium bicarbonate (unlike tricyclics).

3 Paracetamol Poisoning LIVER DAMAGE Occurs because toxic metabolite depletes hepatic stores of glutathione which normally conjugates the metabolite and makes it harmless Unlikely if <150mg/kg paracetamol taken (ie 20 x 500mg tabs in 70kg patient) unless high risk when >75mg/kg can be harmful At risk groups include enzyme inducers eg on anticonvulsants or heavy drinkers; or glutathione depletion eg eating disorders, cyanotic heart disease, children PRESENTATION WITHIN 4 HOURS OF OVERDOSE Activated charcoal if >150mk/kg within 1-2 hours Wait until 4 hours from OD then check plasma paracetamol Give Parvolex if level above treatment line (see BNF for graph) If parvolex started within 10 hours of OD, risk of liver or renal damage is insignificant and patient can be discharged once parvolex complete PRESENTATION 4-8 HOURS AFTER OVERDOSE Too late for charcoal Measure plasma paracetamol level and give parvolex Do not delay if >12g paracetamol ingested and plasma level will not be available within 10 hours (treatment must start within 10 hours for maximum protection) PRESENTATION 8-15 HOUR AFTER OVERDOSE Give parvolex immediately - do not wait for level Measure plasma paracetamol level Stop parvolex if level below treatment line If parvolex continued, liver function (LFT and coag), renal function (U&E) must be monitored, sometimes for up to 3-4 days Safe to discharge after parvolex if INR <2 and not rising, no renal failure and patient is asymptomatic. Otherwise wait until INR falling before sending home If liver damage has occurred advise patient not to drink alcohol for 6 months Continued over

4 PRESENTATION HOURS AFTER OVERDOSE Give parvolex immediately if likely that 12g ingested Measure plasma paracetamol, U&E, LFT and INR Parvolex may be stopped and patient sent home if at 24 hours after ingestion patient is asymptomatic and INR and creatinine are normal and paracetamol level is <10mg/l Otherwise wait until INR and creatinine are falling PRESENTING MORE THAN 24 HOURS AFTER OVERDOSE This is a controversial area Check U&E, LFT, INR and arterial ph Use of parvolex contraversial Discuss with Poisons Unit ADVERSE REACTIONS WITH PARVOLEX 1 in 10 may develop anaphylactoid reaction (flushing/rash) within 1 hour of parvolex administration Stop infusion for 30 minute and recommence at 50mk/kg rate. Give 2mg IV Piriton if required Give subcut adrenalin and nebulised bronchodilators for bronchospasm INCIPIENT LIVER FAILURE If PT >36s (INR >3) at 36 hours there is a 50% risk of fulminant hepatic failure H + >50 and creatinine >300umol/l also predict liver failure Beware hypoglycaemia as cause of coma early in course of extensive hepatic necrosis Give lactulose as prophylaxis against encephalopathy when INR >2 Give vitamin K 10mg IV once only Peak liver necrosis will be reached hours after ingestion. If INR falling by this time, can go home when medically fit If INR deteriorating with signs of encephalopathy, discuss with Liver Unit at Edinburgh Royal Infirmary (short code **020) Continued over

5 INCIPIENT RENAL FAILURE Albuminuria and microhaematuria in first hours suggestive of incipient renal failure Serum creatinine better marker of renal failure than urea when liver damage present Keep careful fluid balance Monitor creatinine daily If develops ARF refer to the Renal Unit Peak renal necrosis at 72 to 96 hours. If no organ damage by this time patient can be discharged PSYCHIATRIC ASSESSMENT Must preceed discharge Ideally should occur within 24 hours of referal